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The Physical, Molecular, and Cellular Basis of Neuromuscular Nociplastic Pain

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 6336

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Guest Editor
Department of Neurology, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA
Interests: acute and chronic neuromuscular pain; myofascial pain; fibromyalgia; pain co-morbidities; the role of the sympathetic nervous system in pain; the role of ion channelopathies in pain; nociceptive and nociplastic pain syndromes
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Special Issue Information

Dear Colleagues, 

The field of pain research has expanded rapidly in the past decade or two, with the number of published studies growing exponentially. Published studies have moved from clinical descriptions of pain disorders to studies of pain mechanisms (including the role tissues and organs play, such as the fascia and spinal cord), of cellular mechanisms (such as the role of glia cells in pain), of molecular contributions to pain (such as the role of ion channels), of cytokines and neurotransmitters, of the role of such central mechanisms (such as central sensitization), and of the role that genetics plays in vulnerability to, and the genesis of, pain disorders. Moreover, there is now great interest in translational research that bridges the gap between new knowledge about cellular and molecular mechanisms of pain and the clinical relevance and usefulness of such research. This Special Issue aims to bring together basic research and the clinical worlds of pain and to point out new directions that research in the field of pain may take. This issue will encompass contributions to acute and chronic pain from the molecular and genetic level to the incorporation of these factors into the development of therapeutic measures.

Dr. Robert D. Gerwin
Guest Editor

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Keywords

  • myofascial pain
  • trigger points
  • fibromyalgia
  • fascia
  • glia
  • neurotransmitters
  • cytokines
  • sympathetic nervous system
  • central sensitization

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Published Papers (1 paper)

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14 pages, 596 KiB  
Concept Paper
A New Unified Theory of Trigger Point Formation: Failure of Pre- and Post-Synaptic Feedback Control Mechanisms
by Robert D. Gerwin
Int. J. Mol. Sci. 2023, 24(9), 8142; https://doi.org/10.3390/ijms24098142 - 2 May 2023
Cited by 11 | Viewed by 5884
Abstract
The origin of the myofascial trigger point (TrP), an anomalous locus in muscle, has never been well-described. A new trigger point hypothesis (the new hypothesis) presented here addresses this lack. The new hypothesis is based on the concept that existing myoprotective feedback mechanisms [...] Read more.
The origin of the myofascial trigger point (TrP), an anomalous locus in muscle, has never been well-described. A new trigger point hypothesis (the new hypothesis) presented here addresses this lack. The new hypothesis is based on the concept that existing myoprotective feedback mechanisms that respond to muscle overactivity, low levels of adenosine triphosphate, (ATP) or a low pH, fail to protect muscle in certain circumstances, such as intense muscle activity, resulting in an abnormal accumulation of intracellular Ca2+, persistent actin-myosin cross bridging, and then activation of the nociceptive system, resulting in the formation of a trigger point. The relevant protective feedback mechanisms include pre- and postsynaptic sympathetic nervous system modulation, modulators of acetylcholine release at the neuromuscular junction, and mutations/variants or post-translational functional alterations in either of two ion channelopathies, the ryanodine receptor and the potassium-ATP ion channel, both of which exist in multiple mutation states that up- or downregulate ion channel function. The concepts that are central to the origin of at least some TrPs are the failure of protective feedback mechanisms and/or of certain ion channelopathies that are new concepts in relation to myofascial trigger points. Full article
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